As explained more fully in the parent application, the CUACT SYSTEM acts to effect lysis and regression of malignant tumors and neoplasms in vivo by depressing the rate of production of adenosine triphosphate (ATP) selectively in cancer cells to a level below that required to maintain cellular viability. Said lethal lowering of the ATP production rate selectively in cancer cells is based upon the general phenomenon that cancer cells are unable to fully utilize glucose, the primary ATP source of normal cells, to generate significant amounts of ATP. Because of their malignant-transformation induced inability to significantly utilize glucose for ATP energy production, cancer cells are almost entirely dependent upon the oxidation of amino acids and fatty acids for production of ATP at rates required for maintenance of viability and proliferation. This metabolic aberrancy of cancer cells is exploited by CUACTS, wherein a Defined Nutritional Regimen (Dnr) is used to minimize dietary amino acid and fatty acid availability to the cancer cells while providing a level of glucose which is adequate for the ATP energy generation needs of normal (nonmalignant) body cells. The Dnr thereby selectively and substantially lowers the maximum available rate at which the cancer cells can produce ATP. Simultaneously, one or more uncoupling agents is administered to effectively uncouple oxidative phosphorylation (O-P uncoupling) in the cell mitochondria, thereby further substantially reducing the maximum rate at which ATP can be produced in the cancer cells. The uncoupling agent, when administered according to a prescribed patient-specific dosage schedule, as more fully described in the parent application, to produce adequate rates of uncoupling, ultimately effects a lethal reduction of the ATP generation rate in the cancer cells selectively. Since the normal cells readily utilize the calorically adequate glucose provided by the dietary carbohydrate source in the Dnr, they experience no net lowering of their ATP-production rate and thus maintain a fully normal rate of ATP production despite the uncoupling action.
It has now been discovered that the oncolytic efficacy of the above-mentioned CUACTS regimen may be lessened in certain cases by high availability of fatty acids mobilized from endogenous sources. The present invention comprises the concomitant clinical in vivo administration, with the CUACTS regimen, of an agent or agents (FAOI) which inhibit fatty acid oxidation in the mitochondria of cancer cells, thereby effecting a direct control over the availability of plasma fatty acids for use in ATP energy production by the cancer cells, regardless of the exogenous (dietary) or endogenous source of the plasma fatty acids.